A型钾离子通道对人舌鳞癌Tca8113细胞增殖的影响

目的:探究A型钾离子(Potassium,K⁺)通道抑制后对舌鳞状细胞癌株(Tca8113)细胞的影响。方法:全细胞膜片钳技术记录和分析A型K⁺通道阻滞剂4-氨基吡啶(4-AP)对Tca8113细胞K⁺电流的影响;MTT检测A型K⁺通道对细胞增殖的作用。结果:在终浓度为2 mmol/L 4-AP作用下,A型K⁺电流的峰值从(267.04±13.84) pA降到(124.81 ±5.24) pA。在一定范围内,不同浓度4-AP能抑制Tca8113细胞在体外的增殖,且抑制程度随药物浓度和作用时间的增加而增强。结论:A型K⁺通道参与Tca8113细胞增殖的过程,且A型K⁺通道阻滞剂能抑制Tca8113细胞的增殖。     

Potassium Channelopathies and Gastrointestinal Ulceration

Potassium channels and transporters maintain potassium homeostasis and play significant roles in several different biological actions via potassium ion regulation. In previous decades, the key revelations that potassium channels and transporters are involved in the production of gastric acid and the regulation of secretion in the stomach have been recognized. Drugs used to treat peptic ulceration are often potassium transporter inhibitors. It has also been reported that potassium channels are involved in ulcerative colitis. Direct toxicity to the intestines from nonsteroidal anti-inflammatory drugs has been associated with altered potassium channel activities. Several reports have indicated that the long-term use of the antianginal drug Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, increases the chances of ulceration and perforation from the oral to anal regions throughout the gastrointestinal (GI) tract. Several of these drug features provide further insights into the role of potassium channels in the occurrence of ulceration in the GI tract. The purpose of this review is to investigate whether potassium channelopathies are involved in the mechanisms responsible for ulceration that occurs throughout the GI tract.     

Suicidal ingestion of potassium permanganate

BACKGROUND:

Potassium permanganate is used clinically as an antiseptic and antifungal agent. Ingestion of potassium permanganate may result in damage to the upper gastrointestinal tract. Burns and ulceration of the mouth, esophagus and stomach occur due to its action. Emergency endoscopy is useful to assess the severity of damage and also to guide management.

METHODS:

We reported a patient presenting to the emergency department after suicidal ingestion of potassium permanganate.

RESULTS:

After treatment, the patient was discharged home on the 7th day after admission.

CONCLUSION:

Early emergency endoscopy should be considered to determine the extent of upper gastrointestinal damage in the emergency department.KEY WORDS: Emergency endoscopy, Gastric damage, Suicide, Potassium permanganate     

人喉癌Hep-2细胞膜钾离子通道与RNA编辑酶1的相关性

目的研究人喉癌细胞系Hep-2细胞膜钾离子通道特性及其与RNA编辑酶1(RNA-dependent adenosinedeaminase1,ADAR1)的相关性.方法以Hep-2细胞为研究对象,采用穿孔膜片钳全细胞记录法研究钾离子通道特性,用逆转录聚合酶链反应检测四乙胺(tetraethylammonium,TEA)阻断钾离子通道前后Hep-2细胞ADAR1 mRNA的表达.结果 Hep-2细胞膜的静息膜电位为(-29.8±1.9)mV,在钳制电压-40 mV,阶跃电压在-80～ 80 mV,记录到一种跨膜电流,该跨膜电流具有电压依赖、外向整流特性,该电流在延迟25ms后最大激活,800 ms内不失活,可被阻断剂TEA阻断.Hep-2细胞钾离子通道被TEA阻断前后ADAR1mRNA相对表达量存在显著性差异.结论 Hep-2细胞膜上存在延迟整流钾离子通道,此钾离子通道可能和ADAR1 mRNA的表达密切相关.     

高浓度快速静脉补钾纠正重症低钾血症（附31例报告）

目的 探讨对重症低钾血症（〈２．１ｍｍｏｌ／Ｌ）患使用高浓度快速静脉补钾的安全性及有效性。方法 在心电图、血钾监测下，用浓度１００￣８００ｍｍｏｌ／Ｌ（即０．８％￣６％）的氯化钾溶液以２５￣４０ｍｍｏｌ／ｈ的速度经外周静脉输注来纠正伴软瘫及不同程度心律失常的重症低钾血症共３１例。结果 采用此法本组病人均在４￣９小时内血钾上升到３．５ｍｍｏｌ／Ｌ以上，心律失常消失，四肢肌力基本恢复。发生１例高钾血     

Nontraditional approaches to the synthesis of some biologically active substituted <Emphasis Type="Italic">p</Emphasis>-benzoquinones

The condensation of mono o- or p-substituted anilines (1) with tetrachloro-1,4-benzoquinone (2) has been achieved by using K₂CO₃ under conventional heating, solid solvent-free grinding, solid-phase microwave irradiation (MWI) conditions to obtain substituted dichloro-p-benzoquinone derivatives (3). All the nontraditional methods described herein provide several advantages over prior methods such as higher yield, convenient work-up procedure, and enviro-economic synthesis. It is observed that solid-supported reaction under MWI is the most appropriate for the synthesis of the title compounds. All the synthesized compounds were tested for their in vitro antibacterial and antifungal activity. Some compounds showed promising antimicrobial properties. The best activity was observed with compounds 3b and 3f. Presented at the International Symposium on Current Trends in Drug Discovery Research (CTDDR) (P-12) 17–21 February 2007, Central Drug Research Institute, Luknow, India. (Abstract Published in Medicinal Chemistry Research 2007, 15(1/6):117–118).     

Intracellular alkalosis stimulates potassium secretion in rabbit CCD

Background. Clinically, it is well known that alkalosis induces hypokdemia, but the precise mechanisms of these interactions between acid-base disturbances and potassium homeostasis are not known with certainty. The role of intracellular alkalosis in the regulation of transepithelial potassium transport was examined in rabbit cortical collecting ducts (CCD). Methods. Intracellular alkalosis was induced by 25 mM N-2 hydroxyethylpiperazine-N′-2-ethanesulfonic acid (HEPES) buffer in which bicarbonate and CO₂ were eliminated. Intracellular pH (pHi) was measured by the load of 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF) dye in principal cells. Isolated CCD was perfused in vitro, and electrophysiological studies and electrolyte transport studies were performed with or without HEPES buffer. Results. Basal pHi in the Krebs-Ringer-Bicarbonate solution was 7.11 ± 0.06. Alkalization by HEPES buffer solution (pH 7.4) resulted in pHi 7.54 ± 0.16. Intracellular alkalization induced by HEPES solution significantly hyperpolarized transepithelial voltage, while net potassium flux increased from −17.3 ± 3.6 to −21.0 ± 3.4 pmol·min⁻¹·mm⁻¹. However, lumen-to-bath isotope sodium flux did not change. The basolateral membrane voltage of the principal cells increased from −74.6 ± 3.0 to −79.6 ± 2.9 mV and transepithelial resistance decreased significantly from 113.1 ± 2.7 to 100.9 ± 20.1 Ω·cm². The calculated fractional resistance of the apical membrane decreased, indicating that intracellular alkalosis increases apical potassium conductance. In the presence of either basolateral ouabain, luminal amiloride, or luminal barium, the HEPES-induced hyperpolarization was preserved. Conclusion. The present study demonstrates that intracellular pH is an important determinant of apical potassium conductance in CCD. Additionally, it should be noted that in the experiments using HEPES buffer solution, intracellular pH in certain epithelial cells was alkalinized by the elimination of bicarbonate and CO₂. Received: April 30, 1998 / Accepted: December 7, 1998     

钾离子通道开放剂停搏液对未成熟心肌电生理特性的影响

目的观察钾离子通道开放剂加入St.Thomas Ⅱ液内,能否改善缺血后未成熟心肌的保护作用.方法未成熟新西兰大耳白兔(2～3周)24只随机分为对照组、处理组和预处理组(各组n＝8),取离体心脏乳头肌标本.对照组充氧台氏液灌注平衡60分,St.Thomas Ⅱ号液灌注停跳30分,充氧台氏液复灌60分.处理组将钾离子通道开放剂Nicorandil加入St.Thomas Ⅱ号液灌注停跳30分.预处理组使用特异性钾离子通道阻滞剂Glibenclamide在平衡期后15分预处理乳头肌标本.利用传统玻璃微电极技术记录心肌细胞动作电位变化.结果①处理组乳头肌停跳后静息电位低于对照组和预处理组,有显著性差异(P＜0.05).②处理组停跳时间短于其他2组,有显著性差异(P＜0.05).③复灌早期处理组50%动作电位时程(APD50、)、90%动作电位时程(APD90)短于停跳前,有显著性差异(P＜0.01),而对照组和预处理组APD50、APD90都明显延长,有显著性差异(P＜0.05),但2组间无显著性差异.④再灌注后处理组动作电位振幅(APA)、动作电位超射值(OS)及动作电位最大复极速度(Vmax)的恢复优于对照组和预处理组,有显著性差异(P＜0.05),而对照组和预处理组间无显著性差异.结论钾离子通道开放剂Nicorandil停搏液可以引起心肌细胞停跳在超极化状态,减轻心肌缺血再灌注损伤,提高再灌注后心肌功能的恢复率.     

The role of dihydropyridine-sensitive voltage-gated calcium channels in potassium-mediated neuronal survival

The survival of isolated neurons from chick embryo ciliary, sympathetic, and dorsal root ganglia is greatly enhanced by concentrations of extracellular potassium that significantly depolarize the neurons (ED50 = 20-25 mM). The survival-promoting effect of elevated potassium on each of these 3 types of neurons appears to be the result of the opening of voltage-gated calcium channels. The dihydropyridine, Bay K 8644, which increases calcium influx through L-type voltage-gated calcium channels in neurons, strongly potentiated the survival-promoting action of elevated potassium (ED50 = 10.8 +/- 7.0 nM). In contrast, chemically closely related dihydropyridines, PN200-110 (ED50 = 0.33 +/- 0.15 nM) and nitrendipine (ED50 = 1.3 +/- 0.3 nM), which block calcium influx through the same voltage-gated channels, completely inhibited potassium-mediated neuronal survival. Chemically different agents that also block calcium influx through voltage-gated channels also inhibited potassium-mediated neuronal survival: the phenylalkylamine verapamil (ED50 = 0.78 +/- 0.38 microM), the benzothiazepine diltiazem (ED50 = 1.7 microM), and the inorganic ion cadmium (ED50 = 5.8 microM). These calcium-channel blockers are not simply toxic to neurons, since they did not inhibit neuronal survival mediated by the neurotrophic proteins, nerve growth factor, basic fibroblast growth factor, or ciliary neurotrophic factor, also suggesting that voltage-gated calcium channels are not involved in the action of these factors. These results suggest that neuronal survival in elevated potassium in ciliary, sympathetic, and dorsal root ganglion neurons is the result of calcium influx through dihydropyridine-sensitive, L-type voltage-gated calcium channels. These findings are discussed in relation to the neuronal toxicity of excitatory amino acids which is also thought to occur through increased calcium influx.     

Tarantula toxins interacting with voltage sensors in potassium channels

Voltage-activated ion channels open and close in response to changes in membrane voltage, a process that is crucial for electrical signaling in the nervous system. The venom from many poisonous creatures contains a diverse array of small protein toxins that bind to voltage-activated channels and modify the gating mechanism. Hanatoxin and a growing number of related tarantula toxins have been shown to inhibit activation of voltage-activated potassium (K_v) channels by interacting with their voltage-sensing domains. This review summarizes our current understanding of the mechanism by which these toxins alter gating, the location of the toxin receptor within K_v channels and the disposition of this receptor with respect to the lipid membrane. The conservation of tarantula toxin receptors among voltage-activated ion channels will also be discussed.